Vascular Flashcards
A 60 year old male smoker has a long history of hypertension & angina. 4 weeks ago he was started on captopril by his GP. His creatinine has increased from 100 to 350 during that time. Renal ultrasound shows that 1 kidney is larger than the other.
A. Medication B. Phaeochromocytoma C. Hyperparathyroidism D. Aortic coarctation E. Hypothyroidism F. Cushing's syndrome G. Acromegaly H. Essential hypertension I. Renal artery stenosis J. Conn's syndrome K. Polycystic kidney disease L. Chronic alcohol excess M. ‘White-coat hypertension’
Renal artery stenosis
Renal artery stenosis is basically narrowing of the renal artery. It occurs typically due to atherosclerosis or fibromuscular dysplasia. The history of smoking, hypertension and angina here are risk factors of the former. The presentation tends to be with accelerated or difficult to control hypertension. Acute kidney injury can be seen after starting an ACE inhibitor or an angiotensin II receptor antagonist. The afferent arteriole is stenosed in RAS and angiotensin II is needed to maintain GFR by constricting the efferent arteriole. ACE inhibitors prevent conversion of angiotensin I to angiotensin II, which is needed to maintain renal perfusion pressure in those with RAS.
There may not be any clinical consequences of RAS – just because someone’s renal arteries are narrowed does not mean they are suffering worsening kidney function, although this may be the case, especially after blockade of the renin-angiotensin system. A definitive diagnosis is made on imaging, where there is some controversy on what is most appropriate to use. USS is safe and non-invasive but the sensitivity and specificity is low. CT/MR angiography has the risk of contrast nephropathy and nephrogenic systemic fibrosis. Conventional angiography (the best test available) has the risk of bleeding and emboli as well as contrast related risks already mentioned.
A 40 year old woman has high blood pressure despite treatment with bendrofluazide & atenolol. Blood tests show Na 140mmol/l, K 3mmol/l, urea 6mmol/l. His bendrofluazide is stopped & he is prescribed potassium supplements, but 2 weeks later his K is still 3mmol/l. Plasma renin activity is low.
A. Medication B. Phaeochromocytoma C. Hyperparathyroidism D. Aortic coarctation E. Hypothyroidism F. Cushing's syndrome G. Acromegaly H. Essential hypertension I. Renal artery stenosis J. Conn's syndrome K. Polycystic kidney disease L. Chronic alcohol excess M. ‘White-coat hypertension’
Correct J. Conn’s syndrome
2) The normal range for potassium 3.5-5mmol/l. You should really know the normal ranges for common values like sodium, potassium and urea by this stage. In Conn’s, potassium is normal or low. It is important when drawing blood to avoid haemolysing the sample, which will cause a falsely elevated potassium level. It is important for screening to calculate the aldosterone/renin ratio, with >30 being suggestive of Conn’s. In Conn’s, aldosterone is raised and renin is low due to negative feedback. This is in contrast to renal artery stenosis where both aldosterone and renin will be raised. It is important to discontinue diuretics and other interfering medications for at least 6 weeks prior to measuring the ratio. The most reliable diagnostic test is a fludrocortisone suppression test. Treatment can be surgical with excision of the adenoma (if aldosterone production is lateralised to one side) or medical with spironolactone and amiloride. There are also familial forms of primary hyperaldosteronism which show an autosomal dominant mode of inheritance.
Spironolactone is an aldosterone receptor antagonist. Amiloride inhibits aldosterone-sensitive sodium channels. They are both examples of potassium sparing diuretics acting on the DCT.
A 45 year old woman is hypertensive & complains that she is putting on weight. On examination, she is centrally obese & has a moon face. There are purple striae on her abdomen. She has glycosuria.
A. Medication B. Phaeochromocytoma C. Hyperparathyroidism D. Aortic coarctation E. Hypothyroidism F. Cushing's syndrome G. Acromegaly H. Essential hypertension I. Renal artery stenosis J. Conn's syndrome K. Polycystic kidney disease L. Chronic alcohol excess M. ‘White-coat hypertension’
3) There is weight gain (truncal obesity), hypertension, moon face and striae in Cushing’s due to hypercorticolism. Cushing’s disease is due to an ACTH secreting pituitary adenoma and is responsible for most cases of Cushing’s syndrome. A low dose 1mg overnight dexamethasone suppresion test can be done, or a 24 hour urinary free cortisol collection to diagnose Cushing’s syndrome. Plasma ACTH should guide further investigation. If ACTH is suppressed, the problem is likely to be with the adrenals. If it not suppressed, pituitary or ectopic disease is more likely.
A 40 year old man is hypertensive & complains that he is putting on weight. On examination he has a prominent jaw and brow. You notice that he is sweating and has large hands and feet. Urine dipstick reveals glycosuria.
A. Medication B. Phaeochromocytoma C. Hyperparathyroidism D. Aortic coarctation E. Hypothyroidism F. Cushing's syndrome G. Acromegaly H. Essential hypertension I. Renal artery stenosis J. Conn's syndrome K. Polycystic kidney disease L. Chronic alcohol excess M. ‘White-coat hypertension’
4) Acromegaly is caused by excess growth hormone and is most often due to a pituitary adenoma. The diagnosis is often made late as the symptoms are insidious in onset. This patient is putting on weight, has prognathism, large hands and feet and glycosuria. There may also be an enlarged nose, soft tissue changes and organomegaly, all as a result of excess GH/IGF-1. Visual impairment may be present is due to the pituitary adenoma putting pressure on the optic chiasm. Tumour mass effect may also cause headaches and there may also be hypopituitarism from stalk compression and CN palsies. IGT and DM are associated and this may result not only in glycosuria but possible polydipsia and polyuria. There may also be altered sexual function, Carpal Tunnel Syndrome and joint dysfunction.
Treatment is either sugical with a transsphenoidal approach, or medical (if the tumour cannot be resected/completely resected) with a somatostatin analogue like octreotide and an adjunctive dopamine agonist like cabergoline. If the patient does not respond to SSAs then pegvisomant which is a GH receptor antagonist can be used, although it is very costly. Gigantism occurs as a result of excess GH during childhood.
A 41 year old woman with a history of neurofibromatosis has erratic BP readings. Some readings are as high as 220/120 where as otheres are normal. She comes to you complaining of intermittent headaches, sweating and palpitations. A. Medication B. Phaeochromocytoma C. Hyperparathyroidism D. Aortic coarctation E. Hypothyroidism F. Cushing's syndrome G. Acromegaly H. Essential hypertension I. Renal artery stenosis J. Conn's syndrome K. Polycystic kidney disease L. Chronic alcohol excess M. ‘White-coat hypertension’
Phaeochromocytoma
5) Phaeochromocytomas presents with paroxysmal episodes of palpitations, anxiety, excessive sweating, pallor and hypertension. It can be inherited in MEN2, von Hippel-Lindau syndrome and NF1. Diagnosis is based on raised urinary and serum catecholamines, metanephrines and normetanephrines. 24 hour urinary VMA will be elevated. CT is used to localise the tumour. Treatment includes medical with the use of phenoxybenzamine, phentolamine and surgical options. Surgical excision is carried out under alpha and beta blockade to protect against the release of catecholamines into circulation when the tumour is being manipulated. The 10% rule is often quoted: 10% are bilateral, 10% malignant, 10% extraadrenal and 10% hereditary.
A 10 year old boy presents with stridor. He reports three episodes of face and tongue swelling, each of which prompted him to report to A&E. There are also red, raised and itchy lesions that cover his body, including face. His sister also suffers from similar attacks.
A. Myocarditis B. Acute rheumatic fever C. Congenital nephritic disease D. Kawasaki disease E. Juvenile idiopathic arthritis F. Congestive cardiac failure G. Primary pulmonary hypertension H. Aortic stenosis I. Pericarditis J. Hereditary angio-oedema K. Toxic synovitis
Correct J. Hereditary angio-oedema
1) This patient has urticaria (erythematous, blanching, oedematous, pruritic lesions) and angio-oedema (swelling). A positive family history of angio-oedema raises a suspicion for a diagnosis of hereditary angio-oedema. There are two forms of this condition. One is manifest by absence of C1 esterase inhibitor whereas the other is due to normal levels of dysfunctional C1 esterase inhibitor. This allows the uncontrolled activation of the complement cascade which therefore gives rise to angio-oedema. This is a condition which is inherited in an autosomal dominant manner although it should be noted that some 50% of cases have no previous FH and are thought to be due to new mutations. Laboratory investigations may reveal a decreased level of C1 and decreased levels or function of C1 esterase which would support the diagnosis. In acquired angio-oedema, C1q levels are low unlike in the hereditary form where it is normal – this differentiates the two forms. The mainstay of treatment is with antihistamines. Airway compromise like the stridor this patient is experiencing is an indication for prompt treatment with adrenaline. The stridor here is a sign of severe laryngeal angio-oedema, which is a sign of impending airway obstruction – this needs to be taken seriously and is an emergency.
A 6 year old girl presents with stiffness and a limp which has lasted for a few weeks now. The onset is reported as insidious and her parents tell you she has not had any injury or infections. One of her knees is swollen and cannot be straightened. The symptoms are worse in the mornings but improve throughout the day. There is also involvement of the small joints of the hands and feet.
A. Myocarditis B. Acute rheumatic fever C. Congenital nephritic disease D. Kawasaki disease E. Juvenile idiopathic arthritis F. Congestive cardiac failure G. Primary pulmonary hypertension H. Aortic stenosis I. Pericarditis J. Hereditary angio-oedema K. Toxic synovitis
Correct E. Juvenile idiopathic arthritis
2) This is juvenile idiopathic arthritis, also known as juvenile rheumatoid arthritis, or Still’s disease. It is the most common chronic arthropathy of children and there are several clinical subtypes. The diagnosis is clinical. Intra-articular steroids offer good control if only a few joints are affected. Methotrexate is also a commonly used disease-modifying agent. More resistant cases are treated with agents which block inflammatory cytokines. Around 10-20% of children with JIA are at risk of developing anterior uveitis and therefore all children with this diagnosis must undergo regular ophthalmological review for inflammation. Remember that symptoms vary according to subtype of disease, which laboratory tests may be useful in classifying. Note also that while this can be called juvenile RA, rheumatoid factor is only positive in a small minority of patients (2-7%).
A 12 year old boy presents with polyarthritis and abdominal pain. He had a sore throat about a week ago. Examination reveals an early blowing diastolic murmur at the left sternal edge. Shortly afterwards, there are bilateral involuntary jerky movements worse when the patient is asked to make a movement.
A. Myocarditis B. Acute rheumatic fever C. Congenital nephritic disease D. Kawasaki disease E. Juvenile idiopathic arthritis F. Congestive cardiac failure G. Primary pulmonary hypertension H. Aortic stenosis I. Pericarditis J. Hereditary angio-oedema K. Toxic synovitis
Correct B. Acute rheumatic fever
3) Chorea features as part of the acute presentation in 5-10% of patients with rheumatic fever. It can also occur as an isolated event up to 6 months after the initial GABHS infection. It is named Sydenham chorea after the doctor who described St Vitus Dance in the 17th century. Choreiform movements can affect the whole body or just one side of the body, in which case it is referred to as hemi-chorea. The head is often involved with erratic facial movements that resemble grimaces, grins and growns, and the tongue may be affected to resemble a bag of worms when protruded, and protrusion cannot be maintained. In severe cases the patient may have an impaired ability to eat. Chorea disappears with sleep and is made worse by purposeful movements. When the patient is asked to grip the doctor’s hand, the patient will be unable to maintain grip and rhythmic squeezing occurs. There are two signs to look out for in these patients. The first is the spooning sign, which is a flexion at the wrist with finger extension when the hand is held extended. The pronator sign is the second which is when the palms turn outwards when held above the head. Both are consistent with chorea.
Remember that the 5 major manifestations of acute rheumatic fever are carditis, polyarthritis, chorea, erythema marginatum and SC nodules – the most common of which are carditis and polyarthritis. The murmur here is a manifestation of carditis. Primary episodes occur mainly in children aged 5-14 and are rare in those over 30. The greatest burden of disease remains in the developing countries and in populations of people living in poverty.
A 16 year old boy presents with 5 month history of chest pain on exertion and two episodes of collapse in the last month. There is also progressive SOB on exertion and now he cannot walk up the stairs without stopping. Examination reveals a loud systolic murmur.
A. Myocarditis B. Acute rheumatic fever C. Congenital nephritic disease D. Kawasaki disease E. Juvenile idiopathic arthritis F. Congestive cardiac failure G. Primary pulmonary hypertension H. Aortic stenosis I. Pericarditis J. Hereditary angio-oedema K. Toxic synovitis
Correct H. Aortic stenosis
4) Aortic stenosis can present with chest pain, dyspnoea and syncope. It is characterised by a harsh ejection systolic murmur heard loudest at the right upper sternal edge at end expiration, which radiates up towards the carotids. The pulse pressure is narrow and there may be an associated slow-rising and plateau pulse. Doppler echo is vital for diagnosis and shows a pressure gradient across the narrowed valve orifice. This is congenital aortic stenosis due to an abnormally formed aortic valve. He may here be considered for surgical repair or TAVR.
A 13 year old girl presents with increasing SOB, particularly when lying down at night to try to sleep. She has also noticed some ankle swelling. Examination reveals a raised JVP, tachycardia and an S3 gallop rhythm on cardiac ascultation. A. Myocarditis B. Acute rheumatic fever C. Congenital nephritic disease D. Kawasaki disease E. Juvenile idiopathic arthritis F. Congestive cardiac failure G. Primary pulmonary hypertension H. Aortic stenosis I. Pericarditis J. Hereditary angio-oedema K. Toxic synovitis
CCF
5) The signs and symptoms this patient has points to CCF (congestive cardiac failure). SOB with orthopnoea due to the sudden increase in pre-load, indicates LV failure. Neck vein distension is also present, which is a major Framingham criteria for diagnosis. Tachycardia and ankle oedema are both minor criteria for diagnosis. Other major criteria for diagnosis include S3 gallop, cardiomegaly and hepatojugular reflux. For all patients, initial investigations should include ECG, CXR, TTE and bloods including BNP levels.
CXR may reveal pulmonary vascular redistribution to the upper zones, Kerley B lines, an increased CTR (cardiomegaly) and pleural effusion. CCF in children occurs as a result of various congenital abnormalities as well as rheumatic fever. Congenital causes include aortic stenosis, PDA and Eisenmenger’s syndrome.
A 70-year-old diabetic male presents with severe pain in his left foot. The pain is present at rest and is alleviated by hanging his leg off the foot of the bed at the night. On examination you note advanced gangrene with superimposed infection of the left foot with absent dorsalis pedis and posterior tibial pulses.
A. Endarterectomy B. Femoro-popliteal bypass C. Antiplatelet drug D. Fasciotomy E. Embolectomy F. Anticoagulation G. Thrombolysis H. Amputation I. Aorto-bifemoral bypass J. Conservative management K. Femoral-femoral crossover graft L. Percutaneous transluminal angioplasty
Correct H. Amputation
1) Gangrene occurs as a complication of necrosis and characterised by the decay of body tissue. It can be due to ischaemia, trauma or infection, or a combination of these processes. There is ischaemic gangrene, which arises due to either arterial or venous obstruction. There is also infectious gangrene which include processes like gas gangrene cause by Clostridium perfringens and necrotising fasciitis which has many causes, commonly Streptococcus pyogenes. Diabetes is a risk factor here and is frequently associated with both infectious and ischaemic gangrene. High blood glucose and impaired immunity, peripheral neuropathy and arterial disease contribute to limb-threatening diabetic foot infections. The absent pulses and symptoms this patient is experiencing here (critical limb ischaemia) also suggests diabetic chronic peripheral arterial disease, which in diabetics tends to affect smaller arteries and affects a younger age group when compared to non-diabetics.There is advanced gangrene here, and in cases of severe limb sepsis, amputation is required. This is a two stage process which at first involves guillotine amputation and later, when the infection has cleared, a definitive amputation and wound closure is needed. If the extremity is not viable (such as a large amount of necrosis, profound anaesthesia/paralysis or an inaudible Doppler pulse) then the patient should undergo prompt amputation. Every effort should be made to preserve as many joints as possible in order to improve rehabilitation chances and to decrease the work of walking around with a prosthesis.
A 55-year-old obese smoker presents with pain in his legs on walking 800 metres, which is immediately relieved by rest. His ankle-brachial pressure index is 0.9.
A. Endarterectomy B. Femoro-popliteal bypass C. Antiplatelet drug D. Fasciotomy E. Embolectomy F. Anticoagulation G. Thrombolysis H. Amputation I. Aorto-bifemoral bypass J. Conservative management K. Femoral-femoral crossover graft L. Percutaneous transluminal angioplasty
Correct J. Conservative management
2) This is peripheral vascular disease with classic symptoms of claudication (in reality, these classic symptoms only occur in a small minority of patients). ABPI should be performed in symptomatic patients and a result less than or equal to 0.9 is diagnostic for the presence of peripheral vascular disease. You need to however bear in mind that this test may not be accurate if the patient has non-compressible arteries (mainly in diabetic patients). This patient has only presented with claudication which is not severely lifestyle limiting. It depends on how much needing to rest every 800 metres or so bothers him. If he does not feel that this is really a functional disability then no additional treatment is required, but follow-up appointments with a doctor should be made to monitor the development of ischaemic symptoms or coronary and cerebrovascular complaints.
If the symptoms are lifestyle limiting then the patient should undergo a supervised exercise programme (only some rather limited quality cohort studies at the moment show an improvement in walking time and symptoms) and medication for symptomatic relief for a period of 3 months. Medication can include cilostazol, pentoxifylline (widely used but no more effective than placebo in RCTs) or naftidrofuryl. Risk factors should also continually be targetted – BP control, statins to lower LDL, beta blockers to target cardiovascular risk and antiplatelet therapy, for instance. If no improvement is made with this regime then patients should be referred to a vascular specialist to have their anatomy defined and assessed for possible revascularisation.
A 65-year-old female presents with sudden-onset pain in her left calf. Although her patient notes are unavailable, she tells you that she is taking digoxin and verapamil for her ‘funny’ heart beat. On examination, the left leg is pale, cold and painful.
A. Endarterectomy B. Femoro-popliteal bypass C. Antiplatelet drug D. Fasciotomy E. Embolectomy F. Anticoagulation G. Thrombolysis H. Amputation I. Aorto-bifemoral bypass J. Conservative management K. Femoral-femoral crossover graft L. Percutaneous transluminal angioplasty
Correct E. Embolectomy
3) Have a think about the differential diagnosis of sudden onset limb pain. Do you remember the 6 Ps of critical limb ischaemia? This patient’s arrhythmia has caused an embolic event, leading to acute limb ischaemia. There is as a result a sudden decrease in limb perfusion with threatened tissue viability. An emergency vascular assessment needs to be done with duplex ultrasound. Treatment depends on whether the patient already has a history of significant atherosclerosis. If so, there will already be a built up collateral supply so there is potentially a longer time window to act and so anticoagulation and thrombolysis are options. Otherwise an embolectomy will be indicated with a Fogarty catheter if there is not a long enough time window. This is typically done by inserting a Fogarty catheter with an inflatable balloon attached to its tip into the offending atery and passing the tip beyond the clot. The balloon is then inflated and then the catheter is withdrawn to remove the clot.
A 63-year-old male with a history of AF underwent an embolectomy a few hours ago after a clot was found in the popliteal artery. He is now complaining of increasing pain and tightness in the treated leg. O/E the leg appears swollen and there is pain on passive flexion of the foot.
A. Endarterectomy B. Femoro-popliteal bypass C. Antiplatelet drug D. Fasciotomy E. Embolectomy F. Anticoagulation G. Thrombolysis H. Amputation I. Aorto-bifemoral bypass J. Conservative management K. Femoral-femoral crossover graft L. Percutaneous transluminal angioplasty
Correct D. Fasciotomy
4) This patient has developed compartment syndrome most likely as a result of soft tissue injury or direct injury to the musculature following the recent embolectomy. Additional causes include fractures and compartment haemorrhage. This condition results from raised interstitial pressure in closed osseofascial compartments. The classical clinical diagnosis will be of the following 6 Ps: pain, pressure, pulselessness, paralysis, paraesthesia and pallor (uncommon). The history here of severe extremity pain and tightness following documented trauma is classical. The pain tends to be out of proportion to the injury and is made worse by passive stretching of the muscle groups which are contained by the affected compartment. Passive stretching of the muscles of the compartment which is involved will also elicit pain. Note that true paralysis is a late sign, as is loss of pulses and pallor. Paraesthesia is however an early seen sign. If the diagnosis is uncertain in an at risk patient then compartment pressure measurement is indicated. Measurements of serum CK and urine myoglobin will also be indicated and these may be elevated with muscle cell lysis and necrosis. This is not due to an occlusive dressing (if it were, the first line treatment would be to remove this dressing). Therefore, a fasciotomy is indicated regardless of time of diagnosis with fasciotomy of all compartments with elevated pressure. There is a clear 6 hour window whereby there are lower amputation and death rates compared to delays >6 hours, so this needs to be done as a matter of urgency. The incision needs to be long enough too! Wound care post-fascitomy is important to prevent the risk of secondary infection and to debride any necrotic tissue, or to consider skin grafts. Post-operatively, care will be MDT with physical and occupational therapies and a range of motion exercises to try an d get the patient fully functional.
A 72-year-old male complains of right leg pain on walking 50 metres. Angiography reveals significant stenosis of the superficial femoral artery.
A. Endarterectomy B. Femoro-popliteal bypass C. Antiplatelet drug D. Fasciotomy E. Embolectomy F. Anticoagulation G. Thrombolysis H. Amputation I. Aorto-bifemoral bypass J. Conservative management K. Femoral-femoral crossover graft L. Percutaneous transluminal angioplasty
Correct B. Femoro-popliteal bypass
6) Broadly speaking, if there is disease with less severe stenosis then endovascular revascularisation is the recommended approach. Surgical revascularisation is recommended if there is more severe stenosis. At this stage, there is no need to get bogged down by the exact recommendations. This significant stenosis will likely require some form of revascularisation. The best option on the list for disease occuring only on one side and localised to the SFA is a femoro-popliteal bypass (colloquially referred to as a fem-pop). Usually the patient’s own long saphenous vein is used as a graft. As you may remember from year 2 anatomy, the SFA becomes the popliteal artery at the popliteal fossa. As a brief summary, femoro-femoral cross-over grafts are done for cases of unilateral iliac artery occlusion. Aorto-bifemoral bypass is used for atherosclerosis of the infrarenal aorta and iliacs.
A 62-year-old lorry driver presents with sudden-onset weakness of the right side of his body as well as ipsilateral loss of vision on the left, which he describes as like a ‘curtain’ descending over his field of vision. His symptoms resolve completely a few minutes later.
Duplex doppler ultrasound CT scan Ankle-brachial pressure index No investigation necessary Venography Contrast angiography Magnetic resonance venography ESR Coagulation studies Brain MRI Blood glucose level EMG walking test Serum CK
Correct Duplex doppler ultrasound
1) This man is presenting with classic features of a TIA. A TIA is colloquially called a ‘mini stroke’ with symptoms typically lasting under an hour (and resolve within 24 hours). An antiplatelet drug such as aspirin is effective secondary prevention if the patient is not already anticoagulated. The patient will be anticoagulated if they have a likely or known cardioembolic source such as AF. Clopidogrel is an alternative in those who do not tolerate aspirin.
The description of transient visual disturbance like a curtain descending over the eye is characteristic of amaurosis fugax. Amaurosis fugax is a transient and painless loss of vision in one eye due to the passage of an embolus into the central retinal artery. The cause could be embolic from the internal carotid artery to cause an occlusion of the ipsilateral retinal artery. Patients presenting with TIAs should be investigated for carotid artery stenosis with a carotid Doppler ultrasound as there is a high risk of having a subsequent full blown stroke. Furthermore if there is a stenosis of >70%, the patient may be a candidate for carotid endarterectomy. Presence of ipsilateral carotid stenosis suggests artery-to-artery embolic event as the cause and this should be the target for surgical or interventional treatment. Follow up tests could be CT angiography or MRA to expand on the abnormal Doppler results. They are not appropriate first line investigations to do here. Head CT is usually normal in TIA. ECG should also be done to investigate for AF which is a common risk factor for embolic cerebral ischaemia.
A 56-year-old man is scheduled for elective AAA repair. The extent and its relationship to the renal arteries need to be identified. Duplex doppler ultrasound CT scan Ankle-brachial pressure index No investigation necessary Venography Contrast angiography Magnetic resonance venography ESR Coagulation studies Brain MRI Blood glucose level EMG walking test Serum CK
CT scan
2) Generally, elective surgical repair is indicated in patients with large symptomatic AAA – repair of aneuryms over 5.5cm offers a survival advantage. Also, young healthy patients and women in particular may benefit from early repair for smaller AAAs. Data suggests that EVAR (endovascular AAA repair) is equivalent to open repair in terms of overall survival but the rate of secondary interventions is higher with EVAR. Generally, those with a greater risk of perioperative morbidity and mortality, such as patients with co-morbidities such as COPD, may benefit from the less invasive approach (anatomy permitting). Younger and healthier patients may benefit from the relative durability of traditional open repair. A CT scan is useful for diagnosis aortic aneurysms which lie close to the origins or or proximal to the renal arteries. While abdominal ultrasound can also identify the AAA and aortic dilation, a CT scan is more useful in localising this lesion and its relationship to the renal vasculature. (‘The juxtarenal abdominal aortic aneurysm: a more common problem than previously realized?’ Arch Surg. 1994;129:734-737)
A 55 year-old man presents with cramping pains in his left leg that occur after walking 100 metres. The pain is effectively relieved by rest.
Duplex doppler ultrasound CT scan Ankle-brachial pressure index No investigation necessary Venography Contrast angiography Magnetic resonance venography ESR Coagulation studies Brain MRI Blood glucose level EMG walking test Serum CK
Correct Ankle-brachial pressure index
3) This is peripheral vascular disease (claudication) and the first investigation to do here is an ABPI. This is an ankle brachial pressure index and has a sensitivity of 95% and a specificity of 100%. It is however important to remember that it may not be accurate in patients who have non-compressible arteries – so beware, particularly in diabetics. Those with either severely stenotic or totally occluded arteries may have a normal ABPI if there is abundant collateral circulation. ABPI of les s than or equal to 0.9 is diagnostic for the presence of peripheral vascular disease. ABPI is performed by taking the systolic pressure of the left and right brachial arteries and the left and right PT and DP arteries pressure. The ABPI is the highest of the DP and PT pressure divided by the higher of the left and right arm brachial artery pressure. Finding the artery with the probe is a skill which may take a bit of practice so have a play around with the probe if you are stuck on a vascular attachment. ABPI is a marker of peripheral atherosclerosis as well as a predictor of vascular events. Risk factors for PVD include smoking, diabetes, old age, hyperlipidaemia and history of coronary or cerebrovascular disease. Treatment is outlined in the explanation for question 2 of the previous EMQ set.
A 65-year-old man is brought into A&E after his son witnessed him collapse in his home. He reveals how his father complained of an excruciating pain in his lower back. On examination, the patient is pale and cold with shut-down perpheries. There is a palpable epigastric mass.
Duplex doppler ultrasound CT scan Ankle-brachial pressure index No investigation necessary Venography Contrast angiography Magnetic resonance venography ESR Coagulation studies Brain MRI Blood glucose level EMG walking test Serum CK
Correct No investigation necessary
4) This is a history of a ruptured AAA. There is back pain here and shut down peripheries and pallor due to blood loss. This patient is in haemorrhagic shock. As this AAA has ruptured, this man will need urgent surgical repair, with of course standard resuscitation measures. Investigations would just waste time. The airway will needed to be managed with supplemental oxygen and ET intubation, a central venous catheter will need to be inserted, an arterial catheter and urinary catheter will also be needed for monitoring, and the target systolic BP is 50-70. Infusing too many fluids may increase the risk of death. The most effective form of surgical repair is an EVAR (endovascular AAA repair), anatomy permitting, otherwise traditional open repair is performed. Open repair has a mortality of 48%. Antibiotics will also be needed to cover bacteria to prevent graft infection. This will be prescribed in line with local protocols.
A 39-year-old multiparous woman presents to the clinic with varciosities in both legs. Although asymptomatic, she wishes to undergo surgery to remove them as they are causing her great embarassment. In order to determine the best treatment plan, the surgeon would like to map out all the incompetent venous pathways. Duplex doppler ultrasound CT scan Ankle-brachial pressure index No investigation necessary Venography Contrast angiography Magnetic resonance venography ESR Coagulation studies Brain MRI Blood glucose level EMG walking test Serum CK
Correct Duplex doppler ultrasound
5) Ablative procedures include stripping and ligation, the aim of which is to permanently remove the varicose vein. Radiofrequency ablation (RFA) can also be done, as well as endovenous laser therapy and foamed sclerotherapy. Phlebectomy or sclerotherapy can also be performed. This is generally reserved for symptomatic cases, although this woman has a cosmetic issue with the appearance of her legs which is causing her distress. There are complications of ablation which the patient will need to be made aware of though, such as bleeding, infection, saphenous nerve injury and neovascularisation.
A duplex ultrasound is the investigation which is required here. It can assess reversed flow and valve closure time. This should be done with the patient standing and with the leg in external rotation for best sensitivity. Specific segments which are affected by reflux can be delineated as the superficial and deep truncal veins, perforators and tributaries can all be visualised. Reflex in the great saphenous or common femoral can be detected with Valsalva while more distal reflux can be elicitied by compressing the leg above the Doppler probe to see if any blood is being forced back towards the feet.
A 50-year-old diabetic lady, who has smoked 40 cigarettes a day for the last 30 years, presents with a year’s history of worsening bilateral calf pain when she walks. The pain goes away when she stops walking but recurs when she resumes. She has been started recently on hormone replacement therapy.
A. Leriche syndrome B. Compartment syndrome C. Baker’s cyst D. Critical limb ischaemia E. Spinal stenosis F. Viable limb G. Deep vein thrombosis H. Rhabdomyolysis I. Dead limb J. Muscle tear K. Acute limb ischaemia L. Intermittent claudication M. Ankylosing spondylitis
Correct L. Intermittent claudication
1) This is peripheral vascular disease with classic symptoms of claudication (in reality, these classic symptoms only occur in a small minority of patients). Remember also that intermittent claudication can also occur in the large muscle groups of the upper leg, which is indicative of narrowing of the deep femoral artery. ABPI should be performed in symptomatic patients and a result less than or equal to 0.9 is diagnostic for the presence of peripheral vascular disease. You need to however bear in mind that this test may not be accurate if the patient has non-compressible arteries (mainly in diabetic patients like this one). If she does not feel that this claudication is really a functional disability then no additional treatment is required, but follow-up appointments with a doctor should be made to monitor the development of ischaemic symptoms or coronary and cerebrovascular complaints.
If the symptoms are lifestyle limiting then the patient should undergo a supervised exercise programme (only some rather limited quality cohort studies at the moment show an improvement in walking time and symptoms) and medication for symptomatic relief for a period of 3 months. Medication can include cilostazol, pentoxifylline (widely used but no more effective than placebo in RCTs) or naftidrofuryl. Risk factors should also continually be targetted – BP control, statins to lower LDL, beta blockers to target cardiovascular risk and antiplatelet therapy, for instance. If no improvement is made with this regime then patients should be referred to a vascular specialist to have their anatomy defined and assessed for possible revascularisation.
